fetal anasarca

7/22/2019 Fetal Anasarca

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Journal of Diagnostic Medical Sonography

27(1) 1925

The Author(s) 2011

Reprints and permission: http://www.

sagepub.com/journalsPermissions.nav

DOI: 10.1177/8756479310392351

http://jdm.sagepub.com

Anasarca is defined as a generalized infiltration of

edema fluid into subcutaneous tissue. The word is

derived from the Greek terms ana, meaning through,

and sark, meaning flesh.1 This generalized edema of

subcutaneous tissue is an ominous finding that is deter-

mined by sonographic examination as >5 mm of tissue

thickness (Figures 13).25

The sonographic appearanceof anasarca frequently gives the anterior abdominal wall

a striking sandwich-like arrangement of thick layers of

fluid-filled connective tissue separating thinner layers of

muscle.6 The presence of fetal anasarca is associated

with severe hydrops fetalis (HF) and the likelihood of

impending fetal demise. However, HF, when found early

in the pregnancy and treated accordingly, may result in

low fetal mortality/morbidity rates. Since HF is often

diagnosed by sonographic examination, it is important

that the sonographer is aware of early fetal sonographic

findings. The purpose of this literature review is to com-

pare and contrast both immune and nonimmune hydrops.Historical research, etiology, diagnosis and associated

findings, clinical implications, and treatment of this con-

dition are discussed.

History

Hydrops fetalis is a condition characterized by any combi-

nation and varying amounts of polyhydramnios, placen-

tal edema, ascites, pleural effusion, pericardial effusion,

and anasarca (Table 1).2,711 This condition was first

documented by Ballantyne12 in 1892. He provided a very

concise description of what is now known as severe HF

but incorrectly hypothesized that the underlying cause

was hereditary. In 1939, Levine and coworkers reported

a link between maternal sensitization to a fetal blood

group antigen and hydrops fetalis.1315 The result was

erythroblastosis fetalis, and the condition was labeled

immune hydrops fetalis (IHF). The following year,Landsteiner and Weiner16 identified the Rh factor as the

sensitizing antigen responsible for IHF. In 1943, how-

ever, Potter17 reported cases where HF was not due to the

antigen immunologic response previously described by

Landsteiner and Weiner. Consequently, the term nonim-

mune hydrops fetalis (NHF) was given to describe those

cases where something other than isoimmunization was

the cause for HF. From that time forward, hydrops fetalis

has been classified into one of two general categories:

immune hydrops fetalis (also known as erythroblastosis

fetalis) and nonimmune hydrops fetalis. Although both

conditions produce similar fetal characteristics, theunderlying causes are quite different and are discussed

separately later.

JDM27110.1177/875479109251a vin

1School of Allied Health, College of Applied Sciences and Arts,

Southern Illinois University, Carbondale, IL, USA2Memorial Hospital of Carbondale, Carbondale, IL, USA

Corresponding Author:

Karen Having, MS Ed, RDMS, RT(R), School of Allied Health, College of

Applied Sciences and Arts, Southern Illinois University, Mailcode 6615,

Carbondale, IL 62901, USA

Email: [email protected]

Fetal Anasarca

Karen Having, MS Ed, RDMS, RT(R)1, and

Stephani Bullock, BS, RDMS, RVT, RT(R)

2

Abstract

Fetal anasarca, defined by the presence of generalized subcutaneous edema measuring >5 mm tissue thickness, is a raresonographic finding associated with end-stage hydrops fetalis and impending fetal death. This literature review describes

the etiology, diagnosis, treatment, and prognosis for both immune and nonimmune hydrops fetalis. Medical technologyand treatment have favorably affected fetal mortality associated with hydrops fetalis. Sonography is a noninvasive

procedure that is heavily used in the management of hydrops fetalis. Sonographic guidance is equally important in thediagnosis and treatment. Sonographer recognition of early signs that may precipitate fetal anasarca is vital to continued

favorable maternofetal outcome.

Keywords

fetal anasarca, hydrops fetalis, nonimmune hydrops

Case Studies


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20 Journal of Diagnostic Medical Sonography27(1)

Immune Hydrops Fetalis

The etiology of IHF is credited to the work of Levine and

Stetson,14 who documented a case study of a woman who

had undergone a transfusion of assumed compatible

blood after the delivery of a stillborn infant and experi-

enced a reaction to the transfusion. Further investigation

revealed the presence of an immune response to an anti-

gen in the mother. It was hypothesized that this response

was due to an antigen present in the father but not in themother. Later researchers were more specifically able to

determine that the immune response occurs as a result of

the mixing of blood from an Rh-negative mother and

Rh-positive fetus. This causes the mother to develop an

immunity that will attack fetal Rh-positive blood cells in

future pregnancies, resulting in the breakdown of fetal

red blood cells and ultimate fetal anemia (erythroblasto-

sis fetalis). The reported incidence of IHF, prior to inter-

ventional treatment availability, was approximately 1%

of all pregnancies.18 Of that number, the Rh antigen was

responsible for 98% of all cases of IHF.8 Rarely, IHF has

been reported to be the result of ABO blood type incom-patibility, which is typically less severe than Rh-negative

reactivity.19,20 In 1968, an Rh immune globulin (RhIG)

was developed to prophylactically counter the maternal

sensitization response responsible for most cases of IHF.

It is estimated that after initiation of RhIG prophylactic

treatment, IHF accounts for approximately 10% of all

reported cases of fetal hydrops. There is currently no

prophylactic treatment available for those cases of IHF

that are caused by atypical antibodies other than Rh.7

Regardless of the underlying cause for IHF (Table 2), the

antigen-antibody reaction is precipitated by a break in the

maternal placental barrier, which allows the mothers anti-bodies to enter the fetal bloodstream. The breakdown of

fetal red blood cells can lead to fetal anemia. Fetal bone mar-

row is primarily responsible for production of red blood

cells, but extensive hemolysis triggers a compensatory

extramedullary hematopoiesis response. Thus, the liver and

splenic tissue is largely overtaken by hematopoietic and

fibroblastic tissue. This results in hepatosplenomegaly. As a

result, normal hepatic metabolic function is impaired, which

can cause portal venous hypertension and eventual fetal

ascites. Concurrently, the edematous placenta becomes

enlarged due to umbilical venous hypertension. The inability

Figure 1. Generalized subcutaneous edema consistent withfetal anasarca.

Table 1. Sonographic Characteristics of Hydrops Fetalis

Polyhydramniosoften the first sonographic finding

Placental edema >5 cm thickness

Ascitesbest viewed between liver and abdominal wall

Pleural and/or pericardial effusiona

Anasarcabgeneralized subcutaneous tissue >5 mm thickness

aFound in varying combination and amounts.bIndicator of chronic/severe hydrops fetalis.

Figure 2. Fetal head circumference measurementdemonstrating fetal anasarca.

Figure 3. Fetal abdominal circumference measurementdemonstrating fetal anasarca.


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Having and Bullock 21

of the fetal liver and placenta to adequately perform protein

synthesis and disperse amino acids leads to fetal hypopro-

teinemia. The fetal response to hypoproteinemia is increased

cardiac output. Depending on the severity of the condition, if

the cardiac output cannot provide adequate fetal tissue oxy-

genation, hypoxia and acidosis occur, which then triggers

capillary dilation and increased permeability. This trio of

physiologic events (hypoproteinemia, increased venous

pressure, and increased capillary permeability) reduces theoncotic pressure and allows for redistribution of the normal

body fluid balance at the intracellular, intravascular, and

interstitial levels into the fetal body cavity (Table 3).4,8

Nonimmune Hydrops Fetalis

NHF, first described by Potter17 in 1943, is the presence

of hydrops fetalis due to underlying factors other than

materno-fetal Rh incompatibility (Table 2). When first

reported, less than 20% of all hydrops fetalis cases fell

into the NHF category. After the introduction and initia-

tion of immunoglobulin prophylaxis for IHF, however,the NHF category has increased to include approximately

90% of all hydrops fetalis occurrences.7,8,20 Although

there is agreement on the percentage of incidence for

NHF, the ratios for incidence range from 1/1500 to

1/4000 pregnancies.7,8,21 Because there is no specific test

to diagnose NHF, careful sonographic screening for fetal

abnormalities is key to early detection and appropriate

treatment.

The underlying etiology of NHF is poorly understood

and has been related to a variety of underlying conditions.22

In North America, NHF is most commonly associated with

cardiac arrhythmias and/or structural malformation.

Cardiac contractility, as a result of abnormal cardiac struc-

ture or function, can lead to heart failure and eventual

hydrops. Chronic or progressive hydrops associated withcardiac structural anomalies is nearly 100% fatal. Outcomes

associated with arrhythmias can often be managed in utero

and will be discussed later. Next most common in occur-

rences is aneuploidy. NHF associated with chromosomal

fetal anomalies is nearly 100% fatal. Hematologic diseases

(especially alpha thalassemia), twin-twin transfusion, and

congenital infections are also commonly cited, although

less frequently, as underlying causes for NHF. With early

detection, this group of conditions has a much better mor-

tality rate. Sohaey7 suggests a survival rate of 75% when

treating for nonimmune fetal anemia after onset of hydrops

compared with 95% when treated prior to development ofNHF. Twin-twin transfusion is associated with high car-

diac output and failure. Fetal congenital infection sources

are numerous, but the most commonly cited is parvovirus.

Fetal infections are commonly associated with myocarditis

and anemia.7,9,23 Multiple other disorders have also been

cited to be associated with NHF. Although not exhaustive,

the list includes cystic hygroma and associated lymphatic

obstructions; thoracic compression (cystic adenomatoid

malformation, diaphragmatic hernia); urinary tract obstruc-

tion, prune-belly syndrome, trisomy 13, 18, and 21; trip-

loidy; Turners 45,X syndrome; TORCH infections;

Table 2. Conditions Associated With Hydrops Fetalis

Immune Hydrops Fetalis Nonimmune Hydrops Fetalis

Maternal Rh incompatibility Other than maternal blood

Maternal ABO incompatibility incompatibility

Abnormal cardiac

structure/function Aneuploidy

Hematologic disease

Twin-twin transfusion

Congenital infections

Cystic hygroma/lymphobstruction

Thoracic compression

Urinary tract obstruction

Prune-belly syndrome

Metabolic disorders

Skeletal dysplasias

Idiopathic

Table 3. Pathophysiology of Immune Hydrops Fetalis

Maternal antibodies enter fetal bloodstream

Antibodies attack and break down fetal red blood cells(hemolysis)

Fetal response is increased blood cell production in bonemarrow (hematopoiesis)

Extensive hemolysis triggers compensatory productionof blood cells in liver and spleen (extramedullaryhematopoiesis)

Liver/spleen are overtaken by hematopoetic andfibroblastic tissue leading to organ enlargement (hepato/splenomegaly)

Livers impaired normal metabolic function leads to portalvenous hypertension

Portal venous hypertension contributes to accumulation offluid in the fetal peritoneum (ascites)

Umbilical venous hypertension produces placental edema

Compromised liver and placental protein synthesis resultin hypoproteinemia

Hypoproteinemia triggers increased cardiac output Severe hypoproteinemia exceeding cardiac output function

causes reduced tissue oxygenation (hypoxia), whichtriggers capillary dilation and increased permeability

Result is redistribution of body fluid balance at intracellular,intravascular, and interstitial levels


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metabolic disorders; and skeletal dysplasias. Despite this

extensive but not inclusive list of underlying etiologies,

NHF is of idiopathic origin in as many as 30% to 80% of

occurrences.7,9,2434 Although dismal outcomes are often

the case, instances of spontaneous resolution of sono-

graphically severe NHF have been reported.3538

A number of nonfetal conditions may be associated

with NHF, although not as prevalent as that of fetal origi-

nation. Those most commonly cited include maternal dia-

betes mellitus, severe anemia and/or hypoproteinemia,

placental chorioangioma, placental venous thrombosis,

and cord torsion, knot, or tumor.7,9,24,39 Because NHF

represents the terminal stage for many conditions, there

is no predictable sequence of events that results in the

transfer of fetal body fluids. Animal studies thus far have

failed to provide the exact reason(s) for the systemic fail-

ures that lead to NHF. Fluid exchange pathways in the

fetus are primarily transplacental, transmembranous, and

transcutaneous. A hydrostatic imbalance allows fluid tocollect in the intravascular, intracellular, and interstitial

compartments. Perhaps transcutaneous exchange is the

major initial pathway until such time as the lymph system

and fetal kidneys can assume adequate fluid elimination

function. There is no consensus on the mechanisms that

result in polyhydramnios and an edematous placenta,

which is almost always present, as well.15,22

Diagnosis of Hydrops Fetalis

The primary intervention for hydrops fetalis prevention is

a thorough prenatal maternal history to include age, racialbackground, occupation, and medical history. This infor-

mation alone may place the pregnancy in a potential high-

risk category. For example, Asians are more prone to

alpha-thalassemia, and sickle cell anemia is more preva-

lent in blacks. School teachers also are more susceptible to

childhood illnesses such as parvovirus B19, rubella, and so

on. Those who are in their teens or older than age 40 years

those taking medications, and those with maternal condi-

tions such as hypertension, diabetes, and systemic lupus

erythematosus are all conditions to be noted and monitored

closely. Family history, including maternal and paternal

genetic information, should also be documented.The mother should undergo a panel of serologic screen-

ing tests to include ABO and blood type, indirect Coombs

test, complete blood count, glucose, TORCH/HPVB19,

VDRL, HIV, IgM, and IgG. Serologic testing can rule out

immune hydrops fetalis with a high degree of accuracy.

There is no maternal serologic test that can produce the same

level of confidence, however, to rule out NHF.

Regardless of the serologic tests, a diagnostic sono-

graphic fetal anatomy screening examination may provide

initial findings consistent with hydrops fetalis and indica-

tions that the pregnancy may be at risk. The pregnancy may

be uneventful in as high as 30% of hydrops fetalis cases.8

One of the first warning signs may be increased uterine

size for pregnancy dating. Polyhydramnios has a recorded

prevalence in up to 75% of fetuses with hydrops fetalis.40

Rarely, however, oligohydramnios is found with underly-

ing NHF conditions such as homozygous alpha-thalasse-

mia and severe lymphangiectasia.8 Placental thickness of

>5 cm is also an abnormal finding and warrants a detailed

fetal anatomy evaluation. In the presence of any of the

above findings, the fetus should be carefully evaluated for

evidence of ascites (best viewed in the space between the

liver and abdominal wall), pericardial and/or pleural fluid,

and cardiac arrhythmia and/or structural abnormality.

Anasarca (generalized edema of fetal subcutaneous tissue

measuring 5 mm or greater) is typically a finding associ-

ated with chronic/severe hydrops and increased mortality

rates. Other sonographic findings that may be encountered

(although not specific to hydrops fetalis) include hepato-

splenomegaly, cardiomegaly, and umbilical vein dilation.2It should be noted that hydrops by definition would include

at least two body cavity fluid accumulations. However,

identification of only one cavity fluid accumulation does

not eliminate hydrops fetalis as a differential diagnosis.22

Prognosis and Treatment

The general prognosis for NHF is dismal. In a series of 79

cases of nonimmune fetal ascites, Favre et al41 report a mor-

tality rate of 78% with ascites diagnosed before 24 weeks

gestation compared with a 45% mortality rate after 24

weeks. Findings consistent with NHF, in addition to ascites,lower survival rates to 33% compared with 49% for those

who do not have the associated findings. Amniotic fluid vol-

ume was not a significant indicator of survival in this study,

ranging from 53% to 33% survival rates for normal amniotic

fluid volume, poly- or oligohydramnios. Hydrops fetalis in

addition to fetal anomalies carries an extreme likelihood for

fetal mortality. Nevertheless, as stated before, there have been

reported cases of spontaneous resolution of NHF.3538

Sonographic-guided amniocentesis for fetal karotype is

beneficial in determining the degree of aggressive treat-

ment. On the other hand, findings consistent with alpha-

thalassemia, infection, glycogen storage disease, ornephrosis will serve to direct appropriate treatment and

delivery plans. Aspiration of fetal cord blood is an alterna-

tive method for obtaining the same results in a quicker time-

frame but with greater risk. Fetal cardiac imaging with

m-mode is useful for determining arrhythmia and cardiac

deformity. Treatment for arrhythmias, in the absence of car-

diac deformity, has produced favorable outcomes with

digoxin, verapamil, adenosine, procainamide, amiodarone,

and flecainide transplacental or direct fetal drug administra-

tion. There have also been limited reports of hydrops rever-

sal with in utero thoracoamniotic shunt placement. This


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procedure is especially indicated to reduce the incidence of

pulmonary hypoplasia. Therapeutic pulmonary effusion

drainage may also be indicated prior to delivery to facilitate

resuscitation. In utero management of twin-twin transfu-

sion does not enjoy a high success rate, but amniocentesis

to reduce fluid volume and embryoscopic laser vessel abla-

tion procedures are being performed with promising out-

comes. In utero antibiotic therapy for infections, especially

parvovirus B19, has proven to be effective, though.2224,4245

There continues to be improved fetal morbidity and

mortality associated with early diagnosis and treatment

with Rh immunoglobulin injections administered with

each pregnancy or invasive procedures during the preg-

nancy. Suggested protocol is RhIG administration at 28

weeks gestation in the unsensitized Rh-negative patient

and another administration postdelivery if the fetus is Rh

positive. Prenatal monitoring may include antibody titers,

amniotic fluid analysis, and serial sonographic fetal

assessment. Depending on the severity of findings, treat-ment can range from minimal postnatal treatment to

intrauterine transfusion.15,18

Fetal anemia can be associated with both IHF and NHF,

necessitating fetal transfusion for survival. Associated

risks for intrauterine transfusion are a point of consider-

ation with a reported 70% to 85% survival rate.24 Middle

cerebral artery Doppler can be used to noninvasively assess

fetal anemia. This procedure requires a high degree of

operator accuracy and cannot yet be considered the gold

standard against fetal blood sampling for the delta optical

density 450 (OD450) bilirubin assessment test.46,47

Delivery of infants affected with hydrops fetalisshould be prearranged at a facility prepared to provide the

necessary care for high-risk infants. The goal is to delay

until 38 weeks gestation or until such time that the risk of

prematurity favors the risk of continued intrauterine

transfusion. There appears to be no consensus on the

preference for vaginal versus cesarean section delivery.

Labor inducement and vaginal delivery are always the

goal and often successfully accomplished. Cesarean

delivery is indicated if breech position or labor is compli-

cated by large fetal and/or placental size, fetal heart rate

variances, and delivery prior to 32 weeks gestation.15,18

Despite overall grim outcomes, good outcomes havebeen reported with hydrops fetalis survivors.48

Maternal Risks

Hydrops fetalis is not without risk to the mother as well.

Polyhydramnios is the most common maternal complica-

tion, which may lead to placental abruption, premature

membrane rupture, and premature labor. Pregnancy-

induced hypertension is the next most common reported

complication, which has the potential to progress to pre-

eclampsia and eclampsia, rendering significant maternal

risk. Other associated maternal complications include

anemia, hypoalbuminemia, and to a lesser degree, uri-

nary tract infections, antepartum hemorrhage, and gesta-

tional diabetes. Invasive procedures provide an increased

risk of placental abruption, and peripartum concerns

include dystocia, cesarean delivery, postpartum hemor-

rhage, and retained placenta.22 On rare occurrences, cases

of Ballantyne syndrome (also known as mirror syndrome

or triple edema) have been reported. Ballantyne syn-

drome is characterized by fetal hydrops, placental

hydrops, and maternal edema. The underlying patho-

physiology of this unusual syndrome is unclear but

believed to be associated with the enlarged placenta.49,50

Conclusion

Fetal anasarca, defined by the presence of generalized

subcutaneous edema measuring >5 mm tissue thick-

ness, is an indication of end-stage hydrops fetalis, andfetal death is the expected outcome. Therefore, early

detection and treatment are a critical fetal morbidity and

mortality component. Adverse outcomes related to IHF

have been significantly reduced via serologic testing,

immunoglobulin therapy, and aggressive in utero treat-

ment. Timing and extent of treatment are largely deter-

mined from ongoing diagnostic sonographic examination

findings.

NHF currently represents approximately 90% of all

hydrops fetalis diagnoses. Because of the wide variety of

etiologies, no specific early warning signs associated

with NHF have been established. A fetal sonographyexamination performed because of a clinical finding of

large for gestational age may be the first indication of

findings consistent with NHF. It is imperative that every

fetal sonography examination is carefully scrutinized for

evidence of polyhydramnios, placental thickening, fetal

ascites, pleural and/or pericardial fluid, and subcutaneous

tissue thickness. Evidence of any of the above should

lead to careful intentional fetal sonographic examination

to rule out associated anomalies.

Sonography is a noninvasive procedure that is heavily

used in the management of hydrops fetalis. Sonographic

guidance is equally important in the diagnosis and treat-ment. Medical technologic and treatment advances have

favorably affected fetal mortality associated with hydrops

fetalis. Thus, fetal anasarca has become a rare sono-

graphic finding. Sonographer recognition of early signs

that may precipitate anasarca is vital to continued favor-

able maternofetal outcome.

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest

with respect to the authorship and/or publication of this

article.


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Funding

The author(s) received no financial support for the research

and/or authorship of this article.

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